Copyright zyxwvutsrqp 0 zyxwvuts 1983 by the Genetics Society of America GENETIC EFFECTS OF UV IRRADIATION ON EXCISION- PROFICIENT AND -DEFICIENT YEAST DURING MEIOSIS MICHAEL A. RESNICK,* JOHN C. GAME** zyxwv AND STANLEY STASIEWICZ" *Cellular and Genetic Toxicology Branch, Notionol Institute of Environmental Health Sciences, Research Triangle Pork, North Carolino 27709, and **Deportment of Genetics, University of Colifornio, Berkeley, California 94720 Manuscript received October 8, 1982 Revised copy accepted April 29, 1983 ABSTRACT The lethal and recombinational responses to ultraviolet light irradiation (UV) by excision-proficient (RAD+) and deficient strains (rad1 zyxw ) of Saccharomyces cerevisioe has been examined in cells undergoing meiosis. Cells that exhibit high levels of meiotic synchrony were irradiated either at the beginning or at various times during meiosis and allowed to proceed through meiosis. Based on survival responses, the only excision repair mechanism for UV damage available during meiosis is that controlled by the RAD1 pathway. The presence of pyrimidine dimers at the beginning of meiosis does not prevent cells from undergoing meiosis; however, the spore products exhibit much lower survival than cells from earlier stages of meiosis. The reduced survival is probably due to effects of UV on recombination. Meiotic levels of gene conversion are reduced only two to three times in these experiments: however, intergenic recombination is nearly abolished after a dose of 4 J/mz to the rod1 strain. Exposure to 25 J/m2 had little effect on the wild-type strain. Since normal meiotic reciprocal recom- bination is generally considered to involve gene conversion-type intermediates, it appears that unrepaired UV damage dissociates the two processes. These results complement those obtained with the mei-9 mutants of Drosophila which also demonstrate a dissociation between gene conversion and reciprocal recom- bination. These results are consistent with molecular observations on the UV- irradiated rod1 strain in that there is no excision of pyrimidine dimers or exchange of dimers during meiosis. HE DNA repair mechanisms that have been identified in mitotically growing T cells of the yeast Saccharomyces cerevisiae can be divided into two categories regarding their role in normal meiosis: essential or dispensable (Cox and PARRY 1968; GAME and MORTIMER 1974; GAME et zyxw al. 1980).Since the excision repair pathway for ultraviolet light (UV) damage induced in yeast does not appear to be required for normal meiosis (SNOW 1968; DICAPRIO and HASTINGS, 1976; DOWLING 1981),it is possible to evaluate, as we have done, the role of the excision pathway in the repair of UV damage during meiosis. In addition, by using mutants of the RAD1 gene, the effects of DNA damage on meiosis can be determined in the absence of excision repair. In the accompanying paper (RESNICK, STASIEWICZ and GAME 1983), we demonstrated that at the doses examined (2 J/m2 or greater) there was no detectable excision of pyrimidine Genetics 104: 603-818 August, 1983.